Abstract
Regulatory CD19+CD24hiCD27+ B cells were proved to be numerically decreased and functionally impaired in the peripheral blood (PB) from rheumatoid arthritis (RA), with the potential of converting into osteoclast-priming cells. However, the distribution and function of CD19+CD24hiCD27+ B cells in RA synovial fluid (SF) were unclear. In this study, we investigated whether RA SF CD19+CD24hiCD27+ B cells were increased and associated with bone destruction. We found that the proportion of RA SF CD19+CD24hiCD27+ B cells was increased significantly, and was positively correlated with swollen joint counts, tender joint counts and disease activity. CXCL12, CXCL13, CCL19 contributed to the recruitment of CD19+CD24hiCD27+ B cells in RA SF. Notably, CD19+CD24hiCD27+ B cells in the SF from RA expressed significantly more RANKL compared to OA and that in the PB from RA. Critically, RA CD19+CD24hiCD27+ B cells promoted osteoclast (OC) differentiation in vitro, and the number of OCs was higher in cultures with RA SF CD19+CD24hiCD27+ B cells than in those derived from RA PB. Collectively, these findings revealed the accumulation of CD19+CD24hiCD27+ B cells in SF and their likely contribution to joint destruction in RA. Modulating the status of CD19+CD24hiCD27+ B cells might provide novel therapeutic strategies for RA.